The inverse myotatic reflex acts to oppose changes in the level of force in the muscle. Just as the stretch reflex can be thought of as a feedback system to regulate muscle length, the inverse myotatic, or group Ib, reflex can be thought of as a feedback system to help maintain force levels in a muscle. With the upper part of the leg as an example, the group Ib reflex arc is depicted in
Fig. 9.7.
The arc starts with the Golgi tendon organ receptor, which senses the tension in the muscle. Golgi tendon organs are located at the junction of the tendon and the muscle fibers and thus lie in series with the muscle fibers, in contrast to the parallel arrangement of the muscle spindles (see
Fig. 9.2 ). Golgi tendon organs have a diameter of about 100 µm and a length of about 1 mm. A Golgi tendon organ is innervated by the terminals of group Ib afferent fibers. These terminals wrap about bundles of collagen fibers in the tendon of a muscle (or in tendinous inscriptions within the muscle).
Hyperactivestretchreflexescanleadtotremorsandclonus,whicharetypesofinvoluntaryrhythmicmovements.Althoughthenegative-feedbackactionofthestretchreflexcanhelpstabilizethelimbataparticularposition,ifanexternalperturbationtothelimboccurs,theconductiondelaybetweentheinitiatingstimulus(musclestretch)andtheresponse(musclecontraction)cancausethestretchreflexcircuittobeasourceofinstabilitythatleadstorhythmicmovements.Specifically,clonusiselicitedbyasustainedstretchofamuscleinapersonwhohasspinalcorddamage.Normally,animposedsustainedstretchonamuscleelicitsanincreaseingroupIaandgroupIIfiberactivity,whichafteradelaycausesacontractioninthemusclethatopposesthestretchbutdoesnotcompletelyreturnthemuscletoitsinitiallengthbecausethegainofthestretchreflexismuchless than1.*
Thispartialcompensation,inturn,leadstoadecreaseingroupIaandgroupIIfiberactivity,whichcausesthelimbtolengthenagain,butnotfully.ThislengtheningonceagainincreasesgroupIaandgroupIIfiberactivity,andsoon.Thedelayisessentialinsettingupthisoscillationbecauseitcausesthefeedbacksignaltocontinueevenafterthemusclehascompensatedandthusresultsinanovercompensationthatleadstothenextovercorrection.However,becausethereflexgainisnormallymuchlessthan1,thisoscillationnormallydiesoutquickly(theovercompensationsdecreaseinamplituderapidly),andthemusclecomestorestatanintermediatelength.Incontrast,whendescendingmotorpathwaysaredamaged,theresultingchangesinspinalcordconnectivityandincreasesinneuronalexcitabilityresultinahyperactivereflex(whichisequivalenttoraisingthegainofthestretchreflexcloseto1).Inthiscase,thesuccessiveovercompensationsaremuchlarger,andanovertbuttransientoscillationcanbeobserved(clonus).Ifthegainequals1,theclonusdoesnotdieoutbutratherpersistsforaslongastheinitialstretchstimulusismaintained.
*Ingeneral,gain ofasystemisdefinedasitsoutputforagiveninput.Inthiscase,theinputtothesystemistheimposedstretch,andtheoutputismovementcausedbythestretchreflex–evokedcontraction.